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Nephrology Boards: Potassium > Hypokalemia > Flashcards

Hypokalemia Flashcards

1
Q

Clinical Manifestations

A

Muscle weakness, rhabdomyolysis, fatigue, ileus, constipation, leg cramps, respiratory difficulty ECG changes: U waves, T-wave flattening, ST-segment depression, arrhythmias, asystole Nephrogenic diabetes insipidus, hypokalemic nephropathy

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2
Q

Clinical Manifestations 40% of patients with hypokalemia also have hypomagnesemia: possible mechanisms:

A

Underlying abnormality/pathology can cause both (e.g., cisplatin, amphotericin, diuretics use, poor dietary intake, diarrhea) Mg2+ is a gate-keeper for ROMK. Low Mg2+ level leaves ROMK open, thus K+ wasting

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3
Q

Clinical Manifestations 40% of patients with hypokalemia also have hypomagnesemia: possible mechanisms:

A

Mg2+ is a cofactor in Na+-K+-ATPase, H+-K+-ATPase Enhanced aldosterone state leading to renal wasting of both cations.

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4
Q

Causes and Mechanisms of Hypokalemia Pseudohypokalemia

A

In vitro (test tube) hypokalemia, not in vivo hypokalemia Pseudohypokalemia may be seen in patients with acute (or chronic) myeloid leukemia due to continuing cellular K+ uptake into rapidly proliferating cells even after the blood is drawn. There may be associated pseudohypoglycemia and hypophosphatemia.

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5
Q

Causes and Mechanisms of Hypokalemia Pseudohypokalemia

A

Seasonal pseudohypokalemia: due to increased intracellular K+ uptake via increased Na+-K+-ATPase activity with transport of blood tubes in warm ambient temperatures

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6
Q

Causes and Mechanisms of Hypokalemia Pseudohypokalemia

A
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7
Q

Causes and Mechanisms of Hypokalemia

Decreased K+ Input

A

Inadequate dietary intake, severe malnutrition (rare due to kidneys’ ability to minimize K+ loss to 5 to 20 mEq/L)

Clay ingestion “geophagia.” Clay binds K+.

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8
Q

Causes and Mechanisms of Hypokalemia

Increased Bodily K+ Loss/Output

A

Gastrointestinal loss: severe diarrhea, vomiting3/nasogastric suction, bowel cleansing (phenolphthalein laxatives, sodium polystyrene sulfonate), acute colonic obstruction, Ogilvie syndrome (acute colonic pseudo-obstruction associated with a secretory diarrhea with very high K+content due to activation of colonic K+ secretion. This condition is associated with various acute illnesses/stressors. Associated electrolyte abnormalities include hypokalemia, hypomagnesemia, and hypocalcemia).

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9
Q

Causes and Mechanisms of Hypokalemia

Increased Bodily K+ Loss/Output

A

Excessive sweats, extensive burns

Dialysis, plasmapheresis

Urinary loss

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10
Q

Causes and Mechanisms of Hypokalemia

Intracellular K+ Shift Due to Increased Extracellular pH

A

Increased extracellular pH (e.g., metabolic or respiratory alkalosis) leads to K+ shifting into cells in exchange for H+ efflux to reduce the extracellular pH.

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11
Q

Causes and Mechanisms of Hypokalemia

NOTE

A

In patients with severe hypokalemia and metabolic acidosis (e.g., patient with proximal RTA), replace K+ to safe level prior to alkalinization!!!

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12
Q

Causes and Mechanisms of Hypokalemia

Intracellular K+ Shift Due to Increased Extracellular pH

A

Increased Na+-K+-ATPase activity:

Insulin administration or endogenous insulin release with glucose administration (e.g., dextrose 5% saline solution)

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13
Q

Causes and Mechanisms of Hypokalemia

Intracellular K+ Shift Due to Increased Extracellular pH

A

NOTE

In diabetic patients with poorly controlled glucose and preexisting life-threatening hypokalemia, provide K+ replacement prior to insulin administration to avoid further fall in preexisting low S[K+]!!!

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14
Q

Causes and Mechanisms of Hypokalemia

Intracellular K+ Shift Due to Increased Extracellular pH

A

Increased β2-adrenergic activity increases cellular K+ uptake: stress, coronary ischemia, delirium tremens, thyroid hormone, β2-agonists (albuterol, terbutaline, dopamine, dobutamine, pseudoephedrine), sympathomimetic stimulants (e.g., amphetamines, high-dose caffeine), theophylline toxicity.

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15
Q

Causes and Mechanisms of Hypokalemia

Intracellular K+ Shift Due to Increased Extracellular pH

A

Inhibition of ATP-dependent K+ channels blocks K+ efflux during repolarization: hypothermia, barium/cesium poisoning, chloroquine intoxication.

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16
Q

Causes and Mechanisms of Hypokalemia

A
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17
Q

Causes and Mechanisms of Hypokalemia

Hypokalemic periodic paralysis:

A

Rare channelopathy (autosomal dominant, varying penetrance):

90% with mutation of the α1-subunit of dihydropyridine-sensitive Ca2+ channel; 10% with mutation of the skeletal muscle Na+ (SCN4A) channel.

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18
Q

Causes and Mechanisms of Hypokalemia

Hypokalemic periodic paralysis:

A

Muscle weakness or paralysis in association with a fall in S[K+]

Upper > lower extremity; proximal > distal weakness

May be associated with hypophosphatemia and hypomagnesemia

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19
Q

Causes and Mechanisms of Hypokalemia

Hypokalemic periodic paralysis:

A

Attacks often begin in adolescence

Triggered by strenuous exercise followed by rest; high-carbohydrate and high-sodium meals or administration of glucose, insulin, or glucocorticoids; sudden changes in temperature, excitement, loud noise, or flashlights

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20
Q

Causes and Mechanisms of Hypokalemia

Hypokalemic periodic paralysis:

Associated conditions:

A

Andersen syndrome: periodic paralysis occurring with either hypo- or hyperkalemia; associated with prolonged QT and sudden death

Thyrotoxicosis due to Graves disease: more common in Asian or Latin/Native American males (propranolol may reverse attacks pending definitive therapy). Of note, patients with thyrotoxicosis hypokalemia periodic paralysis may also have elevated bone alkaline phosphatase for unclear reason.

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21
Q

Causes and Mechanisms of Hypokalemia

Hypokalemic periodic paralysis:

A

Diagnosis: Electromyograms during attacks or with exercise

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22
Q

Causes and Mechanisms of Hypokalemia

Hypokalemic periodic paralysis:

Treatment:

A

Potassium supplement (slow and low dose due to rebound)

If can swallow and breathe adequately: oral KCl, K-citrate, or K-bicarbonate 15 to 30 mEq in 30- to 60-minute intervals as needed.

23
Q

Causes and Mechanisms of Hypokalemia

Hypokalemic periodic paralysis:

A

If cannot swallow and life-threatening: KCl 15 mEq over 15 minutes, then 10 mEq/h in 500 mL dilutant; 5% mannitol dilutant is preferred over normal saline (sodium may worsen condition). Never use glucose (due to endogenous insulin secretion and exacerbation of hypokalemia).

24
Q

Causes and Mechanisms of Hypokalemia

Hypokalemic periodic paralysis:

A

Cardiac monitoring is required with intravenous KCl administration.

Prevention: β2-blockers, K+ supplement, low carbohydrate diet, K+-sparing diuretics, CA inhibitor (acetazolamide)

25
Q

Causes and Mechanisms of Hypokalemia

Increased Renal K+ Loss

A

Recall renal K+ secretion depends on: (1) distal Na+ delivery, (2) generation of transepithelial potential difference (negative lumen) via Na+ entry into ENaC in principal cells at aldosterone-sensitive distal nephron segment, (3) distal urine flow, (4) presence of aldosterone, (5) sensitivity to aldosterone, and (6) kidney mass

26
Q

Causes and Mechanisms of Hypokalemia

Enhanced renal K+ secretion occurs with:

A

Increased distal Na+ delivery to cortical and corticomedullary collecting tubules:

  • Diuretics, high fluid intake/intravenous fluid infusion
  • Bartter and Gitelman syndromes
27
Q

Causes and Mechanisms of Hypokalemia

Generation of transepithelial potential difference (negative lumen) via Na+ entry into ENaC in principal cells at aldosterone-sensitive distal nephron segment is increased:

A

Liddle syndrome

Autosomal dominant, gain-of-function mutation in the β- and γ-subunits of ENaC (PY motif) that reduces the “housekeeping” recognition of ENaC by Nedd4-2 for internalization and degradation, resulting in an increased number of functioning apical ENaC.

28
Q

Causes and Mechanisms of Hypokalemia

Generation of transepithelial potential difference (negative lumen) via Na+ entry into ENaC in principal cells at aldosterone-sensitive distal nephron segment is increased:

Liddle syndrome:

A

Affected patients present with HTN due to excess Na+ retention; hyporenin, hypoaldosteronism due to volume expansion; but hypokalemia and metabolic alkalosis due to facilitated renal K+ and H+ secretion following increased Na+ entry into the undegraded apical ENaC.

Treatment: ENaC inhibition with amiloride. Since this is an end-organ defect, kidney transplantation is curative.

29
Q

Causes and Mechanisms of Hypokalemia

Generation of transepithelial potential difference (negative lumen) via Na+ entry into ENaC in principal cells at aldosterone-sensitive distal nephron segment is increased:

A

Nonreabsorbable anions delivery to collecting tubules can enhance K+ secretion due to the favorable electrical gradient. Additionally, the increased Na+ delivery associated with the anions will also enhance the generation of the favorable electrochemical gradient for K+secretion.

30
Q

Causes and Mechanisms of Hypokalemia

Generation of transepithelial potential difference (negative lumen) via Na+ entry into ENaC in principal cells at aldosterone-sensitive distal nephron segment is increased:

A

Examples of nonreabsorbable anions: bicarbonate (vomiting and proximal RTA), β-hydroxybutyrate in diabetic ketoacidosis, high-dose penicillin/penicillin derivative administration, hippurate from toluene with glue sniffing.

31
Q

Causes and Mechanisms of Hypokalemia

Enhanced renal K+ secretion occurs with:

A

High distal urine flow: high volume intake/infusion, diuretics

Increased mineralocorticoid activity

32
Q

Causes and Mechanisms of Hypokalemia

Increased Renal K+ Loss

Increased mineralocorticoid activity

A

Clinical manifestations: classically seen with triad of hypertension, hypokalemia, and metabolic alkalosis

Mineralocorticoid excess may be categorized as aldosterone dependent, cortisol dependent, or non-aldosterone, non-cortisol dependent

33
Q

Causes and Mechanisms of Hypokalemia

Increased Renal K+ Loss

Increased mineralocorticoid activity

Aldosterone dependent:

A

Secondary aldosteronism:

High renin level leads to aldosterone synthesis.

Source of renin: hypoxia-induced (renovascular hypertension) or unregulated synthesis (renin-secreting tumors)

34
Q

Causes and Mechanisms of Hypokalemia

Increased Renal K+ Loss

Increased mineralocorticoid activity

Aldosterone dependent:

Primary aldosteronism:

A

Aldosterone synthesis is independent of renin levels.

Sources of aldosterone: adrenal hyperplasia, adenoma, or carcinoma, glucocorticoid-remediable aldosteronism

35
Q

Causes and Mechanisms of Hypokalemia

Increased Renal K+ Loss

Increased mineralocorticoid activity

Aldosterone dependent:

Primary aldosteronism:

Glucocorticoid-remediable aldosteronism:

A

Autosomal dominant with formation of a chimeric gene due to unequal crossover of sequences at meiosis, where the hybrid gene contains both the promoter of 11-β-hydroxylase enzyme (enzyme for cortisol synthesis) and aldosterone synthase gene (enzyme for aldosterone synthesis)

36
Q

Causes and Mechanisms of Hypokalemia

Increased Renal K+ Loss

Increased mineralocorticoid activity

Aldosterone dependent:

Primary aldosteronism:

Glucocorticoid-remediable aldosteronism:

A

Stimulation of the promoter with ACTH upregulates both cortisol and aldosterone synthesis. Recall that aldosterone is normally upregulated by angiotensin II.

37
Q

Causes and Mechanisms of Hypokalemia

Increased Renal K+ Loss

Increased mineralocorticoid activity

Aldosterone dependent:

Primary aldosteronism:

Glucocorticoid-remediable aldosteronism:

A

Clinical manifestations: early moderate to severe HTN, hemorrhagic stroke and ruptured aneurysms (brain MRA every 5 years after puberty has been recommended), normo- to hypokalemia (the former due to the diurnal variation of ACTH).

38
Q

Causes and Mechanisms of Hypokalemia

Increased Renal K+ Loss

Increased mineralocorticoid activity

Aldosterone dependent:

Primary aldosteronism:

Glucocorticoid-remediable aldosteronism:

A

Diagnosis: genetic testing for crossover between aldosterone-synthetase and 11-β-hydroxylase; biochemical evaluation: suppressed plasma renin activity and high serum aldosterone, increased levels of 18-hydroxy-cortisol, ACTH and 18-oxo-cortisol.

39
Q

Causes and Mechanisms of Hypokalemia

Increased Renal K+ Loss

Increased mineralocorticoid activity

Aldosterone dependent:

Primary aldosteronism:

Glucocorticoid-remediable aldosteronism:

A

Treatment: glucocorticoid (to suppress ACTH) or mineralocorticoid receptor antagonism (spironolactone, eplerenone) ± ENaC antagonism (amiloride) to counteract the effect of excess aldosterone.

40
Q

Causes and Mechanisms of Hypokalemia

Increased Renal K+ Loss

Increased mineralocorticoid activity

Cortisol dependent: (cortisol has mineralocorticoid activity)

A

Sources of cortisol: excess production (Cushing’s); reduced inactivation of cortisol to cortisone by the enzyme 11-β-hydroxysteroid dehydrogenase type 2 11-βHSD2).

41
Q

Causes and Mechanisms of Hypokalemia

Increased Renal K+ Loss

Increased mineralocorticoid activity

Cortisol dependent: (cortisol has mineralocorticoid activity)

A

Reduced 11-β-hydroxysteroid dehydrogenase activity:

  • Licorice: glycyrrhizic acid and its hydrolytic product, glycyrrhetinic acid, from licorice are potent competitive inhibitors of 11-βHSD2.
  • Mutation of 11-βHSD2: Syndrome of apparent mineralocorticoid excess (AME)
42
Q

Causes and Mechanisms of Hypokalemia

Increased Renal K+ Loss

Increased mineralocorticoid activity

Non-aldosterone, non-cortisol dependent:

A
  • Liddle syndrome
  • Deoxycorticosteroid excess (associated with congenital adrenal hyperplasia)
43
Q

Causes and Mechanisms of Hypokalemia

Increased Renal K+ Loss

Increased mineralocorticoid activity

Non-aldosterone, non-cortisol dependent:

A

Activating mutation of mineralocorticoid receptor (MR):

  • Autosomal dominant disorder where the MR is constitutively activated
  • Hypertension may worsen with pregnancy due to progesterone
  • Spironolactone (normally an MR antagonist) now acts as an agonist!
44
Q

Causes and Mechanisms of Hypokalemia

Evaluation of Mineralocorticoid Excess in patients with Triad of HTN, Hypokalemia, and Metabolic Alkalosis:

A
45
Q

Causes and Mechanisms of Hypokalemia

Others

Amphotericin B:

A

This is a multiplanar molecule that is lipophilic on the outside and hydrophilic on the inside. The molecule inserts itself into tubular cell membrane and acts as an ionophore, allowing electrolytes to flow in the direction of favorable chemical gradient.

46
Q

Causes and Mechanisms of Hypokalemia

Others

Amphotericin B:

A

The formulation of liposomal amphotericin covers up the lipophilic surface of amphotericin and reduces its insertion into tubular membranes, thus minimizing intracellular electrolyte losses into the urinary space and back-leak of H+ into circulation.

47
Q

Causes and Mechanisms of Hypokalemia

Others

Amphotericin B

A
48
Q

Causes and Mechanisms of Hypokalemia

Others

A

Magnesium deficiency can lead to K+ wasting at the thick ascending limb of loop of Henle. Mg2+ is a “gate-keeper” against K+ exit via ROMK into the lumen.

49
Q

Causes and Mechanisms of Hypokalemia

Others

A

Salt-wasting nephropathies, tubular injuries (tubulointerstitial diseases, cisplatin, aminoglycosides), acute monocytic or myelomonocytic leukemia with lysozyme-induced tubular injury leading to K+ wasting)

50
Q

Causes and Mechanisms of Hypokalemia

Others

A

Hypercalcemia (inhibits ROMK in thick ascending limb of loop of Henle and induces a form of nephrogenic diabetes insipidus).

51
Q

Causes and Mechanisms of Hypokalemia

Others

Management of Hypokalemia: Routine Considerations

A

If S[K+] < 3 mEq/L, STAT ECG, cardiac monitor

If safe, avoid glucose-containing solutions until life-threatening hypokalemia has been corrected.

52
Q

Causes and Mechanisms of Hypokalemia

Others

Management of Hypokalemia: Routine Considerations

A

If safe, avoid correction of hyperglycemia with insulin administration until life-threateninghypokalemia has been corrected.

If safe, avoid alkalinization until life-threatening hypokalemia has been corrected.

53
Q

Causes and Mechanisms of Hypokalemia

Others

Management of Hypokalemia: Routine Considerations

A

Use central lines if >10 mEq/h replacement is needed.

Consider femoral line over internal jugular or subclavian line if >20 mEq/h replacement is needed to avoid cardiac irritation.

Check magnesium levels and replace as necessary.

Nephrology Boards: Potassium (4 decks)

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